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为了解糖尿病对输精管平滑肌功能的影响及其机理,我们比较了链脲菌素(streptozotocin)所致糖尿病大鼠及共同龄对照组大鼠输精管平滑肌对电场刺激,氯化钾,去氧肾上腺素的反应及钙通道的改变。电场刺激引起的收缩反应是单收缩之后继以连续性收缩。糖尿病组单收缩幅度较大,两组连续收缩几乎相同。1μmol/L Bay K8644使糖尿病鼠输精管产生单收缩,对照组无影响。氯化钾引起的收缩和钙内流在两组都增强,但在1 μmol/L Bay K8644存在时,糖尿病组比对照组增加明显。10μmol/L去氧肾上腺素引起的收缩可完全被0.1μmol/L硝苯啶阻断。100μmol/L新霉素在对照组可完全抑制去氧肾上腺素引起的收缩,但在糖尿病组只能部分抑制,并使单收缩增强。用钙通道拮抗剂配体[~3H]PN200-110所做的结合实验表明,对照或糖尿病组钙通道的亲和力和结合位点的数量都没有明显的不同。在输精管可溶性成分中,蛋白激酶C含量在糖尿病组是对照组的两倍。这些结果提示在没有神经病变及钙通道数量不变的情况下,氯化钾增强链脲菌素所致糖尿病大鼠输精管的收缩反应部分是由于钙通道开放的概率和蛋白激酶C活性增强所致。
To understand the effect of diabetes on vas deferens smooth muscle function and its mechanism, we compared the effect of vas deferens smooth muscle in streptozotocin-induced diabetic rats and common-age control rats on electrical stimulation, potassium chloride, phenylephrine Response and changes in calcium channels. Electric field stimulation induced contractile response is contracted after a single contraction. Diabetic group contraction amplitude larger, two groups of continuous contraction is almost the same. 1μmol / L Bay K8644 produced a single contraction of the vas deferens in diabetic rats, but no effect in the control group. Potassium chloride-induced contractions and calcium influx increased in both groups, but increased significantly at 1 μmol / L Bay K8644 compared with the control group. Contraction induced by 10 μmol / L phenylephrine was completely blocked by 0.1 μmol / L nifedipine. Neomycin at 100μmol / L could completely inhibit phenylephrine-induced contractions in the control group, but only partially inhibited in the diabetic group and enhanced the contractions. Binding experiments with the calcium channel antagonist ligand [~ 3H] PN200-110 showed no significant differences in the calcium channel binding affinity and the number of binding sites in the control or diabetic group. Among the soluble components of vas deferens, the protein kinase C content in diabetic group was twice that of the control group. These results suggest that in the absence of neuropathies and unchanged numbers of calcium channels, potassium chloride potentiates the vasoconstrictor response of streptozotocin-induced diabetic rats partly due to the increased probability of calcium channel opening and increased activity of protein kinase C .